Animal studies have shown that bioassayable vasopressin activity is released into the blood stream in response to the administration of angiotensin II (AII). The purpose of the proposed project is to determine whether radioimmunoassayable vasopressin (ADH) is released in human subjects in response to angiotensin II infusions and, if so, whether this response can be blocked by the angiotensin II analogue, saralasin, as our preliminary experiments appear to indicate. The possibility that AII may be the mediator of the ADH response to such physiological stimuli as dehydration, elevation of plasma osmolality by hypertonic saline infusions, reduction of "central" volume by assumption of the upright posture and pharmacologically induced arterial hypotension will be tested by determining: (a) whether rises in plasma and urinary ADH can be correlated with rises in plasma renin activity in any or all of these circumstances and (b) whether saralasin and the converting enzyme inhibitor, Captopril, will block ADH release in response to any or all of these physiological stimuli. The potential clinical significance of a role of AII in mediating the stimulus to ADH release will be tested by observations in patients with various types of edema (cirrhosis with ascites, congestive heart failure, idiopathic edema, nephrosis) after administration of a water load, after assumption of the upright posture and after Captopril administration.